The COVID-19 pandemic continues around the world, where the United States is among the worst in terms of both morbidity and fatality of the viral infection. We aim to investigate the plausible link of tissue SARS-CoV-2 viral entry gene expression, such as TMPRSS2 and ACE2, with infection and death by gender during the COVID-19 pandemic in the United States. We find a significantly higher incidence of COVID-19 death in men than in women, even though SARS-CoV-2 infection in women is higher than in men. We discover that the expression of TMPRSS2 and ACE2 in intestine, but not in lung, tends to be positively associated with the incidence of SARS-CoV-2 infection in men. In contrast, the high incidence of death in men is negatively correlated with TMPRSS2/ACE2 expression in intestine. Strikingly, the correlation of TMPRSS2/ACE2 expression with SARS-CoV-2 infection and death is the opposite in females, compared with that in males. Interestingly, male hormone signaling seems to be involved in mortality, as the low expression of testosterone receptor AR in the prostate contributes to death in men according to age. These observations point to a plausible contribution of male hormone metabolism in the regulation of TMPRSS2/ACE2 signaling to fatality by SARS-CoV-2 infection in men.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8618612 | PMC |
http://dx.doi.org/10.3390/pathogens10111378 | DOI Listing |
J Med Internet Res
January 2025
Division of Surgery & Interventional Science, Faculty of Medical Sciences, University College London, London, United Kingdom.
Background: The literature is equivocal as to whether the predicted negative mental health impact of the COVID-19 pandemic came to fruition. Some quantitative studies report increased emotional problems and depression; others report improved mental health and well-being. Qualitative explorations reveal heterogeneity, with themes ranging from feelings of loss to growth and development.
View Article and Find Full Text PDFMenopause
January 2025
Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Objective: Although dysregulated inflammation has been postulated as a biological mechanism associated with post-acute sequelae of severe acute respiratory coronavirus 2 (SARS-CoV-2) infection (PASC) and shown to be a correlate and an outcome of PASC, it is unclear whether inflammatory markers can prospectively predict PASC risk. We examined the association of leukocyte count and high-sensitivity C-reactive protein (hsCRP) concentrations, measured ~25 years prior to the coronavirus disease 2019 (COVID-19) pandemic, with PASC, PASC severity, and PASC-associated cognitive outcomes at follow-up among postmenopausal women.
Methods: Using biomarker data from blood specimens collected during pre-pandemic enrollment (1993-1998) and data on 1,237 Women's Health Initiative participants who completed a COVID-19 survey between June 2021 and February 2022, we constructed multivariable regression models that controlled for pertinent characteristics.
PLoS One
January 2025
Department of Critical Care Medicine, West China Hospital, Sichuan University, Chengdu, China.
Background: The relationships between pectoralis muscle parameters and outcomes in patients with coronavirus disease 2019 (COVID-19) remain uncertain.
Methods: We systematically searched PubMed, Embase, Web of Science and the Cochrane Library from 1 January 2019 to 1 May 2024 to identify non-overlapping studies evaluating pectoralis muscle-associated index on chest CT scan with clinical outcome in COVID-19 patients. Random-effects and fixed-effects meta-analyses were performed, and heterogeneity between studies was quantified using the I2 statistic.
PLoS One
January 2025
Department of Pharmacology & Toxicology, The University of Texas Medical Branch, Galveston, Texas, United States of America.
Severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1) and -2 (SARS-CoV-2) are beta-coronaviruses (β-CoVs) that have caused significant morbidity and mortality worldwide. Therefore, a better understanding of host responses to β-CoVs would provide insights into the pathogenesis of these viruses to identify potential targets for medical countermeasures. In this study, our objective is to use a systems biology approach to explore the magnitude and scope of innate immune responses triggered by SARS-CoV-1 and -2 infection over time in pathologically relevant human lung epithelial cells (Calu-3/2B4 cells).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!